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47 sats \ 15 replies \ @Lux 28 Feb \ on: Fun Fact Friday - Best Fun Fact Gets 5,000 CCs meta
Fenbendazole, originally designed to cure parasites, selectively blocks the synthesis of microtubules by binding to β-tubulin. This action stops the polymerization of tubulin dimers in parasite cells, leading to their death. Surprisingly, fenbendazole, along with other benzimidazoles, exhibits similar effects against tumor cells. Today, it is believed that fenbendazole kills cancer through three main mechanisms:
1. Apoptosis Induction - cancer cell cycle arrest and cytotoxicity
2. Inhibition of Glucose Uptake in Cancer Cells - malignant cells are known for their high glucose uptake, consuming glucose 200 times faster than ordinary cells
3. Reactivation of the p53 Gene - the strongest tumor suppressor in our bodies
https://www.fenbendazole.org/fenbendazole-information/how-fenbendazole-works/
Sounds more like a wishful thinking than anything else.
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wash your ears
References
Lacey, E. (1974). The benzimidazole anthelmintics—a review
Patel, K., & Bhuyan, R. (2021). Antitumor activity of albendazole against the human colorectal cancer cell line
Choi, S. H., Martinez, M. N., & Weatherly, L. M. (2018). Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways
Johnston, M. D., & Read, A. F. (2018). Repurposing anthelmintic drugs as cancer treatments: perspectives from evolutionary biology
Morris, G. M., & Keppler, D. (2019). The role of anthelmintic drugs in the treatment of cancer
Mukhopadhyay, T., Sasaki, J., Ramesh, R., & Roth, J. A. (2018). Antitumor effects of fenbendazole: A possible role of microtubule disruption
Lacey, E., & Morrell, A. (2013). Benzimidazoles in cancer therapy: repurposing anthelmintics for oncology
Pedersen, P. L. (2013). Hexokinase II: Cancer’s double-edged sword acting as both facilitator and gatekeeper of malignancy when bound to mitochondria
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Have you read these references? If it used in the clinics?
p53 can carry various mutations in different places. I know about some drugs in the clinical trials targeting y220c mutation for the protein reactivation, still miles from approval, often with serious side effects. All the other mutations (or most of them) are considered undruggable.
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most clinics do not know what the fuck they are doing. the health providers in most clinics have been heavily indoctrinated. why do all domesticated mammals undergo a deworming procedure yearly, except humans? oh right, people are supposed to fast... but they DON'T, ever since break-fast became the "most important sugar-rich meal of the day!"
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Feel free to deworm yourself if you think this is a good idea… if e.g. you eat a lot of raw uncooked food.
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The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53–p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins. We also observed a reduction of cell viability and changes of cellular morphology corresponding to mitotic catastrophe, i.e., G2/M cell cycle arrest of large multinucleated cells with disrupted microtubules.
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TIL
Mitotic catastrophe has been defined as either a cellular mechanism to prevent potentially cancerous cells from proliferating or as a mode of cellular death that occurs following improper cell cycle progression or entrance
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Ok, so I was wrong with the mutations. Fenbendazole is supposed to block the interaction between p53 and its regulator Mdm2. Good luck with that. Many inhibitors from nutlins to don’t know what have failed in the clinics so far. Mostly because of serious side effects. Can fenbendazole spare the healthy cells?
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I am sorry but what is this paper supposed to show? That there is some effect in a cell culture on a petri dish?
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